Fig. 1: Design and characterization of catalytic activity tunable CNPs that protect against chemotherapy-induced AKI.

a Schematic illustration of catalytic activity tunable CNPs with context-dependent cytoprotective activities for AKI prevention during chemotherapy. High-concentration of chemotherapeutics in the kidneys induces AKI by producing excessive reactive oxygen species (ROS). In the renal cortex, the administered ultrafine CNPs are switched “on”, and could counteract toxic ROS to prevent AKI. In the tumor acidic microenvironment, CNPs would be switched “off” by the high-level H⁺, and exert no effect on intratumoral ROS, maintaining the efficacy of chemotherapy. b TEM image of ultrafine CNPs in chloroform, scale bar: 50 nm. Insert: high-resolution TEM image of CNPs, scale bar: 2 nm. c TEM image of ultrafine CNPs after DSPE-PEGlyation in water, scale bar: 50 nm. Insert: hydrodynamic diameter distribution of DSPE-PEGlyated CNPs. d The oxygen (O₂) production of CNPs under different pH conditions (pH 7.4, pH 6.6, and pH 6.0) during the reaction with H₂O₂. Data are presented as mean values ± SEM., n = 3 independent experiments. e Raman spectra of CNPs at different time points in each cycle of reaction with H₂O₂ under different pH conditions (pH 7.4 and pH 6.0). f Schematic illustration of the context-dependent catalase-like activity of CNPs under different pH conditions (pH 7.4 and pH 6.0). V_O, oxygen vacancy. In b–c, experiments were repeated three times independently. Source data are provided as a Source Data file.